[!TIP] Mnemonic:
LPFB - P looks like R -> Right axis deviation
LAFB - LA - Left Axis Deviation
LBBB - also left axis deviation

| Causes Left Axis Deviation | No effect on axis |
| Affects MI diagnosis | No effect on MI diagnosis|
| Best seen in V6 - M pattern| Best see in V1 - RSR pattern|
the 'best seen' lead views the heart from the same side as the blocked bundle.

[!INFO] Shortcut to diagnosing BBBs
Another simple way to diagnose a left bundle branch in an ECG with a widened QRS complex (> 120 ms) would be to look at lead V1.

• If the QRS complex is widened and downwardly deflected in lead V1, a left bundle branch block is present.
• If the QRS complex is widened and upwardly deflected in lead V1, a right bundle branch block is present.Source (i.e take that to mean "if there is anything above the baseline in V1")
  

• Preexisting LBBB makes diagnosis difficult:
  • Diagnosis of MI and left venctricular hypertrophy in patients with prexisting LBBB is difficult.

[!INFO] ECG criteria for LBBB:

1. QRS duration greater than 120 milliseconds
2. Absence of Q wave in leads I, V5 and V6
3. Monomorphic R wave in I, V5 and V6
4. ST and T wave displacement opposite to the major deflection of the QRS complex
   Source

• QRS duration > 0.12 seconds
• RSR pattern in V1 and V2 (with second R wave usually larger than the first)
• Downsloping ST segments with T inversion IN V1 and V2.
• Broad S wave in V5 and V6, I and aVL.
• RBBB does not afect the cardiac axis.

• Treated with topical antibacterial, miconazole and if severe, oral erythromycin.

Dermatofibroma

Neurologic:

• Slow relaxing reflexes Source - Woltman sign

The classic finding is subacute combined dengeneration (SACD) of the spinal cord.

• This leads to demyelination of the dorsal and lateral white matter. (i.e tracts).
• Leading to sensory (paraesthesia, sensory ataxia) and motor (weakness, spacticity, paraplegia and incontinence).
• Shrunken spinal cord with discoloration of the posterior and lateral columns Source

[!INFO] What is 'combined'?

• Combined refers to combined degeneration of the dorsal and lateral white matter tracts of the spinal cord due to demyelination. -UpToDate. Source
• In B12 deficiency, there is also associated peripheral neuropathy.

• Neuropathic features are commoner in B12 deficiency than in B9 deficiency.

Signs

• Motor signs due to spinal cord demyelination:

  • Weakness, ataxia which may progress to spasticity and paraplegia.

• Sensory signs due to spinal cord demyelination:

  • Paraesthesia
  • posterior columns first -> then lateral columns (some sources say pain an temperature are spared) Source

• Peripheral neuropathy:

  • Sensory: Neuropathy is symmetrical, involves legs > arms and causes paraesthesia and gait problems. (in Glove and stocking distribution)
  • Motor: loss of reflexes

• Therefore, there is a peculiar pattern of reflex loss:

  • Loss of reflexes (lower motor sign) with up-going Babinski reflex. (upper motor sign)

• Advanced neurologic changes include irritability, paranoia, delirium and confusion.

• There may also a "lemon tinge" of sclera.

• Acquired thrombophilia - venous AND / OR arterial
• Patients can also have livedo reticularis and thrombocytopenia
  Management:
• Primary prophylaxis is with aspirin.
• Secondary prophylaxis with warfarin - PassMedicine
• Anticoagulation during pregnancy.

Thiazide diuretics bind to the chloride receptor of the Na-Cl cotransporter in the DCT and inhibit it's function causing urinary loss of Sodium and Chloride.

• Telcagepant - newer drug. (prevents blocks the binding of CGRP to receptors within the areas of the central and peripheral nervous system and prevents pain transmission)

[!TIP] Mnemonic: TET
Like a "TET" spell
Triptans, erogatamine, Telcagepant
Acute -> Agonist (fewer letters, quicker to say)
- Verapamil - can cause headache on it's own but reduced migraine frequency.
- Cyproheptadine - 5HT2 receptor antagonist; also has antihistamine activity.

• "oh bee" -> "eh bee" (Ob -> Ab)

[!INFO] All Three sensory modalities affected!
Eyes, ears, Nose

• Clinical symptoms of Refsum diseasemay develop from infancy to adulthood and include progressive retinitis pigmentosa, peripheral polyneuropathy, cerebellar ataxia, sensorineural deafness, ichthyosis, anosmia, and cardiac conduction defects.
• Presents in late childhood or adolescence.
• There is lower limb atrophy.
• #autosomal-Recessive
• See also [[Genetics Notes#NARP]]
• 

Anatomy of the CNIII nucleus

Cranial nerves in intracranial hypertension

The cranial nerves most commonly affected by intracranial pressure are the

1. Abucent nerve (VI) - lateral rectus palsy
2. Trochlear nerve (IV) - palsy of superior oblique
3. Oculomotor nerve (III) - 'Down and out' pupil.
   Source

Mechanisms:

• The abducent nerve and trochlear nerve are injured 'because of their long intracranial course'. Also the abducent nerve can also be stretched due to increased ICP as it enters the Dorello canal . Source
• The oculomotor nerve is injured due to direct compression during temporal lobe uncal herniation.
  

Abducens nerve

Causes of abducens nerve palsy:
Source
Source

• SOLs
• Infection (lyme disease, syphillis, tuberculosis, cryptococcus)
• Lesions of the petrous apex : Basal skull fracture, complicated otitis media, sinus thrombosis.
• in the cavernous sinus: Cavernous sinus thrombosis, ICA aneurysm, cavernous sinus fistula
• CN VI palsy is frequently seen as a postviral syndrome in younger patients
  • and as an ischemic mononeuropathy in the adult population.

Source
Source

Trochlear nerve

• Commonest cause of palsy is traumatic.
• Diabetes can also cause palsy.
• Presentation:
  • Patient complains of vertical or torsional diplopia.
  • Affected eye is tilted up (hypertropia)
  • patient keeps head tilted to the opposite direction
• Diagnosis: head tilt test. (tilting head to the side of the lesion causes the hypertropia to increase.
• Source

• Phagocytosis of the coagulative necrotic area starts after about 3 days and continues upto 7 days. (Tissues are most vulnerable to rupture)
• Scar formation is complete by 8 weeks, the scar has formed.

Carey coombs - Coombs for carditis

• Cryoglobulinaemia most commonly affects females in 40s and 50s.
• They can present with puprura, arthralgia and leg ulcers, polyneuropathy and hepatic involvement - probably due to vasculitis?
• Type 1:
• causes symptoms due to vascular obstruction by the precipitate:
  • eg; digital ischemia, livedo reticularis, skin necrosis, purpura (due to vasculitis) , Raynaud phenomemon - specially with cold temperatures.
• Type 2:
  • Meltzer's triad - Purpura, Arthralgia, Weakness.

1. All patients should be on aspirin and statin.

• There are 5 main groups of antianginal drugs.
  • 1 and 2 are first line.
  • Others are second line.
  • See the numbered list below.
    
    Source
• First line anti anginals: BB and CCB. They can be alternated or combined.
• Second line antianginals: Long acting nitrates, ivabradine, nicorandil, ranolazine
  • Of these, nitrates and nicorandil are last line (according to the diagram above)
  2. Why too much intracellular calcium is bad:
  3. Ranolazine can cause QT prolongation. Source
  4. Mnemonic: NiKOrandil (නිකන් ඉන්නවා -> relaxing -> smooth muscle relaxant action)

ACEi can be used to prevent ACS in aginal patients. Source

• Rheumatoid arthritis with Intralpumonary nodules.
• ⭐

    - Widening of QRS > 100ms is associated with an increased risk of seizures whilst QRS > 160ms is associated with ventricular arrhythmias - passMedicine
- 

• Dialysis is ineffective.
• Many other antiarrhythmics are contraindicated because they affect the action potential in counterproductive ways (i.e can worsen the problem)

1. **Primary idiopathic**
2. **Primary immune complex mediated** - eg. Goodpasture's syndrome (Goodpasture's has less recurrence than GPA - PasTest answers); From the image above, *these are small vessel vasculitidies*. 
    5. Cryoglobulinaemic vasculitis (CryoVas)
    6. ?Behcet' disease
    7. 

2. Secondary

• They are Granulomatous diseases

[!INFO] The distinction between GCA and Takayasu is made mainly base on patients age!
Because histologically, they are very similar.

• Young patient -> Takayasu
• Old patient -> GCA

• there is no muscle damage: creatine kinase is normal. (i.e it's myalgia, not myopathy)

[!INFO] Diagnosis:
ESR and biopsy are very suggestive for PMR but both can be falsely negative!

- One of which is the **temporal artery**. 
- Other arteries: *ophthalmic*, *occipital*, **vertebral**, *posterior ciliary*
- Can also cause *mononeuritis mulitplex*. [Source](https://emedicine.medscape.com/article/316024-overview#showall)
- *However*, *ESR can be normal* in upto 20%; Therefore, normal ESR doesn't exclude GCA. 

• Definitive Dx : temporal artery biopsy. Patchy lesions -> >1cm needs to be examined.
  • Halo sign on colour doppler is suggestive of the disease.
• Affects the largest vessels in the body: the aortic arch and it's branches or the more distal aorta and branches. (in about 1/3)
  • Distal branch involvement -> renal artery stenosis and hypertension, bowel ischemia, leg claudication etc.
  • It can cause aortic root dilation which can cause AR.
• Pulmonary arteries are involved in 50%
• There is transmural scarring and thickening with significant luminal narrowing.
• AKA pulseless disease or aortic arch syndrome.
  
• (eg, bruit, especially carotid; blood pressure difference of extremities, difference in pulse volume, claudication, hypertension)
• Steroids are the mainstay.
• Diagnosis: MR angiogram.
• Post prandial abdominal pain, diarrhoea, GI haemorrhage. Also ?abdominal bruits.
• Tenderness over affected arteries like carotid arteries.
• 1/3 of patients have chronic hepatitis B infection.
• Occurs in middle aged men; associated with severe systemic symptoms.
• Fibrinoid necrosis of vessel walls -> thrombosis and infarction.
• Probably immune complex mediated (as it's sometimes associated Hepatitis B).
• Involves ==small arteries within the organs==.
  1. Frequency of involvement : Kidney > heart > liver > GI tract
  2. Somehow, lungs aren't involved.
  3. Renal: haematuria and proteinuria.
     1. Renal involvement is due to luminal narrowing and ischemia of renal arterioles but not due to glomerular inflammation or necrosis.
     2. Renal arterial aneurysms and renal infarctions
  4. Coronary arteritis causing MI.
  5. Liver
  6. Bowel ischemia -> acute abdominal pain, necrosis and bleeding
  7. Mononeuritis mulitiplex - vaso vasorum infarctions
  8. Skin - subcutaneous haemorrhage and gangrene

Treatment: Corticosteroids +/- azathioprine.

• ECG: widened QRS, AV block, ventricular arrhythmias
• Increased cellular metabolism due to uncoupling of cellular respiration causes hypoglycaemia. (neuroglycopenic symptoms can occur even when CBS is in the normal range).
• Almost identical to cinchonism (quinine toxicity).
• In terms of management however, whereas aspirin can be cleared from overdose victims by haemofiltration, quinine cannot be extracted easily by extracorporeal methods. Central nervous symptoms such as tinnitus, deafness and visual defects which may occur with aspirin are usually transient whereas quinine leaves permanent neural damage, if the patient survives.
• Quinine toxicity is managed by urgent alkalinization with bicarb and intubation + hyperventilation.

[!INFO] Indications for defibrillation
"unstable" should be taken to mean any of the follwing:

1. Shock
2. Syncope
3. Evidence of myocardial ischemia
4. Heart failure (pulmonary oedema)

• From a passmedicine answer. No other good reference but it seems reasonable.

gentisic -> gentleman -> black suit